Nephrocalcinosis

Nephrocalcinosis may be caused by a variety of things, including underlying disorders or conditions, medications or supplements, and infections. Causes may include:^[1][2]

• Primary hyperparathyroidism 
• Distal renal tubular acidosis (RTA)
• hypervitaminosis-D states (very levels of vitamin D)
• Other cause of hypercalcemia (increased calcium in the blood)
• Sarcoidosis 
• Phosphate supplementation
• Medullary sponge kidney
• Osteoporosis due to immobilization, menopause, aging, or steroids
• Primary (familial) hyperoxaluria, or secondary hyperoxaluria
• Chronic disorders such as Bartter syndrome, primary hyperaldosteronism, Liddle syndrome, and 11-beta hydroxylase deficiency
• Autosomal dominant hypophosphatemic rickets and X-linked hypophosphatemic conditions
• Premature birth 

Other causes may include the use of certain medications such as acetazolamide; tuberculosis of the kidney; and infections related to AIDS.^[1]

Nephrocalcinosis may have a variety of causes, including underlying disorders, certain medications and supplements, and infections. Nephrocalcinosis itself is not inherited. However, the condition causing nephrocalcinosis in an individual may be inherited. Some inherited conditions that may be associated with nephrocalcinosis include:^[1][2][3]

• Multiple endocrine neoplasia type 1 (MEN1)
• Familial distal renal tubular acidosis
• Chronic granulomatous disease
• Primary hyperoxaluria
• Bartter syndrome
• Alport syndrome
• Primary hyperaldosteronism
• Liddle syndrome
• 11-beta hydroxylase deficiency
• Autosomal dominant hypophosphatemic rickets and X-linked hypophosphatemic conditions
• Williams syndrome 
• Beta thalassemia 

Treatment of nephrocalcinosis includes treating the underlying condition causing nephrocalcinosis, if it is known. The goal of treatment is to reduce symptoms and prevent more calcium from being deposited in the kidneys. Measures are usually taken to reduce abnormal levels of calcium, phosphate, and oxalate in the blood. Medications that cause calcium loss are typically stopped.^[1]

Treatment of hypercalcemia (increased calcium levels in the blood) and hypercalcemic nephropathy typically includes adequate hydration by isotonic sodium chloride (normal saline) solution to reverse hypercalcemia and protect the kidneys. Treatment of macroscopic nephrocalcinosis (calcium deposition that is visible without magnification) may include thiazide diuretics and dietary salt restriction, potassium and magnesium supplementation, and citrate supplementation in idiopathic hypercalciuria (of unknown cause) and in distal renal tubular acidosis. Lessening of nephrocalcinosis may occur over time, but in many cases, such as when it results from primary hyperoxaluria or distal renal tubular acidosis, nephrocalcinosis is largely irreversible. Therefore, early detection and treatment are important.^[2]

Individuals interested in learning about treatment options for themselves should speak with their health care provider or a nephrologist.